Inhibition of natural transformation by bacteriophages of Streptococcus pneumoniae
The gram positive bacterium Streptococcus pneumoniae (the pneumococcus) causes severe human diseases such as pneumoniae, septicaemia and meningitis. In Europe, S. pneumoniae is the main cause of community-acquired pneumonia where mortality rates reach 20% in cases accompanied by bacteraemia [1]. S. pneumoniae is competent for natural transformation, a process by which it can uptake DNA from its environment and incorporate it in its genome [2]. Transformation allows the pneumococcus to evade the vaccine by changing capsular serotypes, leading to the emergence of successful non-vaccine type strains, and plays a critical role in the acquisition of antimicrobial resistances (AMR) [3]. Together, this severely impairs treatment and prevention of pneumococcal infections, and resistant S. pneumoniae are considered a serious threat by the CDC [4]. Understanding the pathways that lead to acquisition of AMR and virulence properties by S. pneumoniae is crucial for developing better preventive and therapeutic measures, as well as for fighting the spread of AMR. Clinical isolates of S. pneumoniae often carry integrated phages. During their life cycle temperate phages integrate into the bacterial chromosome where they normally reside dormant until their activation is triggered. In naturally transformable bacteria, phages are at risk of being deleted from the chromosome if their host acquires DNA from a non-lysogenic strain. We are currently investigating various mechanisms by which phages protect themselves from the threats of DNA uptake. Students will have the opportunity of learning and using a wide-range of molecular techniques, such as cloning, PCR, RNA sequencing, RT-qPCR, electrophoresis, protein expression, Western Blots and transformation assays. The project will be conducted under the supervision of Geneviève Garriss, assistant professor at the department of Microbiology, Tumor and Cell Biology. 1. Kadioglu A, et al. 2008. Nat Rev Microbiol 6:288-301. 2. Straume D, et al. 2015. Infect Genet Evol 33:371-80. 3. Weinberger DM, et al. 2011. Lancet 378:1962-73. 4. CDC. https://www.cdc.gov/drugresistance/biggest_threats.html. Accessed 2019-09-09. |